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Antisense-induced blockade of GATA-3 expression could inhibit Th2 excursion of tumor cells in vitro and in vivo.

Abstract
Previous studies have shown that tumor cells predominantly express Th2 type cytokines and transcription factors. GATA-3, as a Th2-specific transcription factor, plays a central role in positive-regulating Th2 development. So whether the expression of GATA-3 in tumor cells has any effect on tumor development is a question of interest. In the present study, we inhibited the expression of GATA-3 in tumor cells through antisense RNA blockade technique, and observed its effects on tumor in vitro and in vivo. Our results showed that antisense GATA-3 treatment could inhibit the expression of TNF-alpha and Th2 cytokines in tumor cells, and antisense-induced blockade of GATA-3 could also depress tumor growth in tumor-bearing mice. We suggest that the ratio of T-bet/GATA-3 can be evaluated as a more important marker of the status of Th1/Th2 type. And our results might provide some evidence about the molecular regulatory mechanisms in tumor cell development.
AuthorsDongzhu Yao, Xiaojun Zhang, Haiming Wei, Zhigang Tian
JournalCellular & molecular immunology (Cell Mol Immunol) Vol. 2 Issue 3 Pg. 189-96 (Jun 2005) ISSN: 1672-7681 [Print] China
PMID16212886 (Publication Type: Journal Article)
Chemical References
  • Cytokines
  • GATA3 Transcription Factor
  • RNA, Antisense
  • Tumor Necrosis Factor-alpha
Topics
  • Animals
  • Cell Line, Tumor
  • Cloning, Molecular
  • Cytokines (metabolism)
  • GATA3 Transcription Factor (biosynthesis, deficiency, genetics, metabolism)
  • Gene Expression Regulation
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Neoplasms (immunology, metabolism, pathology)
  • RNA, Antisense (genetics, metabolism)
  • Spleen (metabolism)
  • Th1 Cells (immunology, metabolism)
  • Th2 Cells (immunology, metabolism)
  • Transfection
  • Tumor Necrosis Factor-alpha (metabolism)

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